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Session 145 Poster Abstracts
Morbidity and Mortality from Hepatitis C in the HIV-Infected Population
Session Day and Time: Wednesday, 1:30 - 3:30 pm
Poster Hall


879    
Hepatitis C/HIV-1-co-infection in Long-term Non-progressors
Pedro Castro*, M Laguno, F García, M Plana, E Fumero, M Nomdedeu, T Gallart, J Mallolas, J Miró, and J Gatell
Hosp Clin, Univ of Barcelona, Spain

Background:  It has been reported that long-term non-progressor (LTNP) HIV-1-infected patients have better in vitro responses against hepatitis C virus (HCV), which could lead to a better evolution of the hepatitis C. On the other hand, HCV and its treatment (interferon = ribavirin) could influence evolution of HIV-1 infection in LTNP.

Methods:  A case-control (1:2) study comparing co-infected LTNP (n = 22) vs co-infected HAART-treated normal progressors (matched by sex, age, and HCV genotype) (n = 44) was performed. The variables analysed were signs of hepatopathy (clinical status, AST, ALT, GGT, alkaline phosphatase, albumin, bilirubin, platelet count, liver structure and presence of spleenomegaly in echography, inflammation, and fibrosis in liver biopsy), response to HCV treatment, HIV viral load and lymphocytes T subsets. A cohort of LTNP with (n = 28) vs without HCV infection (n = 7) was also compared to assess the influence of HCV on HIV-1 infection.

Results:  Liver enzymes (AST, ALT and GGT) were lower in the LTNP group than in normal progressors (p <0.05). There were no statistically significant differences between LTNP and normal progressors in clinical signs of hepatopathy, presence of hepathomegaly at physical examination (60 vs 67%, p = 0.67), echostructure (normal in 66 vs 51.85%, p = 0.76) or grade of inflammation in liver biopsy >3 of 6 in 42.8 vs 42.3%. Grade of fibrosis in live biopsy was lower in LTNP than normal progressors >2 of 4 in 14.28 vs 48.14%, p = 0.10). There were no differences in the response to HCV treatment between groups (57.1% vs 50% of viral sustained response). However, LTNP presented proportionally a higher drop of CD4 during HCV treatment, that was sustained after 2 years of discontinuing it (–229, 4, and –61cells/mm3 HCV-treated LTNP (n = 7), normal progressors (n = 44), and non-HCV-treated LTNP (n = 15), respectively, p <0.05). Of 7 LTNP, 2 needed HAART after HCV treatment because of immunologic impairment. There were no statistically significant differences in CD4+/CD8+ T cells, and HIV-1 viral load when LTNP HCV+ were compared with LTNP HCV­.

Conclusions:  LTNP do not seem to have a better evolution or response to treatment of HCV infection than normal progressors. However, HCV treatment, but not HCV infection, could have a deleterious effect on evolution of LTNP.